Front Matter (PDF) - Blood

‘B.W & C0#{174} PRODUCTS 

FOR LEUKEMIA 

‘LEUKERAN’#{174} brand 

CHLORAMBUCIL 

FOR THE TREATMENT OF CHRONIC LYMPHOCYTIC LEUKEMIA 

AND MALIGNANT LYMPHOMAS 

ADVANTAGES: ‘Leukeran’ brand Chlorambucil has been found easier to handle than nitrogen mustard 

and some other related drugs because it produces fewer side effects and is not as damaging to the 

hemopoietic system in therapeutic doses. 

CAUTION: ‘Leukeran’ brand Chlorambucil is a potent drug. Blood counts should be taken once or twice 

weekly. Discontinue or reduce the dosage upon evidence of abnormal depression of the bone marrow. 

Radiation and cytotoxic drugs render the bone marrow more vulnerable to damage and ‘Leukeran’ brand 

Chlorambucil should not be used within 4 weeks of such therapy. During the first 3 to 6 weeks of 

chlorambucil therapy, it is recommended that white blood cell counts be made 3 or 4 days after each 

of the weekly complete blood counts. While it is not necessary to discontinue chlorambucil at the first 

evidence of a fall in neutrophil count, it must be remembered that the fall may continue for ten days 

after the last dose and that as the total dose approaches 6.5 mg./ Kg. there is a risk of causing irreversible 

bone marrow damage. Whenever possible avoid use during first trimester of pregnancy. 

SUPPLIED: Bottles of 50 tablets. 

‘MYLERAN’#{174} brand 

BUSULFAN 

FOR THE TREATMENT OF CHRONIC GRANULOCYTIC LEUKEMIA 

ADVANTAGES: ‘Myleran’ brand Busulfan is more selective than nitrogen mustard or the folic acid 

antagonists in its effect on myeloid cells, and may be somewhat safer to use. The drug has been found 

especially useful for patients in whom radiotherapy has been abandoned, but this does not necessarily 

mean that it is always of value when radiotherapy has failed. 

CAUTION: ‘Myleran’ brand Busulfan is a potent drug. Use of the drug should be restricted to patients 

for whom complete blood counts are available at intervals of at least one week. Most careful hematological 

control is essential, since large doses may produce irreversible depression of the bone marrow 

which may not become obvious for 4 to 6 months. Whenever possible avoid use during first trimester 

of pregnancy. 

SUPPLIED: Bottles of 25 tablets. 

PURINETHOL’#{174}brand 6MERCAPTOPURINE 

FOR THE TREATMENT OF ACUTE LEUKEMIA 

AND CHRONIC GRANULOCYTIC LEUKEMIA 

ADVANTAGES: Administered orally, this drug has resulted in prolongation of life in a substantial proportion 

of patients suffering from acute leukemia. Remissions may be either complete or partial and 

vary in duration from only a few weeks to a year or longer. 

SIDE EFFECTS: Nausea, vomiting and anorexia are uncommon but may occur as the result of overdosage. 

Toxic effects such as gastrointestinal irritation or ulceration of mucous membranes are rare. 

CAUTION: ‘Purinethol’ brand 6-Mercaptopurine is a potent drug. Blood counts should be made weekly. 

At the first sign of depression of bone marrow the drug should be withdrawn or dosage reduced. Jaundice 

has been observed in some instances, suggesting possible liver damage. It is suggested that if toxic 

hepatitis develops, 6-Mercaptopurine be withheld, since jaundice has been reported to disappear in 

some cases when the drug is discontinued. Whenever possible avoid use during first trimester of 

pregnancy. 

SUPPLIED: Bottles of 25 and 250 tablets. 

Complete literature available on request from Professional Services Dept. PML. 

J.t3 BURROUGHS WELLCOME & CO. (U.S.A.) INC., TUCKAHOE, N. Y.

BLOOD: THE JOURNAL OF HEMATOLOGY 

111 

What’s the difference between thromboplastins? 

REPRODUCIBILITY 

in both the normal and the therapeutic range 

To be reproducible in the prothrombin time test the thromboplastin must be... 

Precontrolled . Standardized . Stable 

I 

HOW DOES YOUR THROMBOPLASTIN RATE? 

Are tissue source and conditions of extraction identical in every 

lot prepared? Do particle size and number meet exact specifications? 

Does every lot have optimal ionic strength, pH? 

Does it cause normal plasma to clot in a specified time? 

Will the prothrombin times of anticoagulated plasmas 

follow a predictable curve? 

Is it free of phenol, formaldehyde or sodium azide (all known enzyme 

hibitors that may falsely extend prothrombin time)? Can it be frozen 

without loss of activity? Is packaging adequate to protect it from 

deterioration due to heat and humidity? 

If you answered “no” to any one of these questions, it’s time you 

compared your thromboplastin with others, If you answered 

“yes” to all these questions you’re using 

Si 

rn p1 a sti fl#{174},1’5 

incomparable. 

GENERAL 

WARN 

ER-CHILCOTT 

DIAGNOSTICS 

Thie 

One

BLOOD 

The Journal of Hematology 

NOTE TO CONTRIBUTORS 

Papers are accepted for publication on condition that they are contributed solely to this Journal. 

Manuscripts must be typewritten, in good English, double or triple spaced, on good quality bond 

paper with at least one inch margins, the original and one duplicate submitted (figures and tables 

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are advised to examine issues of the Journal so that their manuscripts will conform to the 

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Publishers, 2130 South 17th St., Sheboygan, Wis., or 381 Park Avenue South, New York 16, N. Y. All 

communications concerning editorial matters should be addressed to Dr. \Villiam Dameshek, Harrison 

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Agents for Great Britain: H. K. Lewis & Co., Ltd., 136 Cower Street, London, W.C. 1. 

Published monthly at 2130 South 17th St., Sheboygan, Wis. Second class postage paid at Sheboygan, 

Wisconsin. 

COPYRIGHT © 1964 by G S GRUNE & STRATTON, INC.

When the need 

for iron is acute.. 

inject 

Astrafer#{174}(Atra) 

(dextriferron) 

intravenously 

Side Effects: In exceptionally sensitive patients, 

flushing of the face, followed by a sensation of’ 

warmth throughout the body may be seen. Such 

reactions are proportional to the speed of injection 

and disaear momentarily. 

Precautions: Inject Slo’.Vly; not more than 5cc, In 

2 minutes. Patient should be made to rest 15 to 30 

minutes after each injection. If expected results are 

not obtained after administration of the calculated 

amount, a complicating illness should be 

suspected and therapy dIscontinued. A second 

course is not indicated in the absence of provd, 

massive, intercurrent hemorrhage. 

Contraindications: Pernicious anemia, hemotytic 

anemia, chronic leukemia, bone marrow 

depression and ,liver damage. 

Consult manufacturer’s literature before using. 

Write for literature and 

professional sample. 

ASIIA Pharmaceutical Products, Inc. 

Worcester 6, Massachusetts

BLOOD: THE JOURNAL OF HEMATOLOGY Vii 

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DADE REAG:ENTS INC. #{149}MIAMI 35,’FLORIDA

vu’ BLOOD: THE JOURNAL OF HEMATOLOGY 

By George E. Cartwright, M.D. 

Diagnostic Laboratory Hematology 

Third Edition, Revised and Enlarged 

“The appearance of a new edition of a well-known text is something 

which usually is to be greeted with enthusiasm. This definitely is true 

concerning the third edition of Cartwright’s book. One of the most useful 

technique books available for the hematology laboratory, the newly 

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including laboratory directors, hematologists, technologists, 

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352 pages #{149} 66 illustrations #{149} $8.75 

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LEUKEMIA 

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This new report on a subject of increasing 

clinical importance explores many of 

the new findings in hematology that 

affect leukemia. It remains the definitive 

work for today’s practitioner. Said Lancet 

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- . - this book is a classic work.” 

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The miniature cell was designed specifically for the new membrane. Together, they reduce separation 

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Actually the MicroZone Electrophoresis System is an extension of the time honored Model R System. 

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x BLOOD: THE JOURNAL OF HEMATOLOGY 

Seminars in Hematology 

HEMAT 

1crE9,1AIES0 

N 

 

JS 

ifl 

Editor in Chief, Peter A. Miescher, M.D. 

Assistant Editor, Jamshid Javid, M.D. 

SEMINARS IN HEMATOLOGY is the clinician’s answer to 

the problem of keeping effectively informed. The first 

two issues (Vol. 1, Nos. 1 and 2) feature important 

papers on multiple myeloma. In the July issue is an 

informative seminar on megaloblastic anemias and for 

October the editors have scheduled a discussion of 

coagulation. Don’t miss these helpful papers, designed 

to give a clear and authoritative picture of subjects 

of clinical importance. 

A 

Four issues per year, approximately 96 pages per 

isue. Subscriptions for 1964: $8.00 per year ($9.00 

outside the U.S.A.). Single issues: $3.00 ($3.50 

outside the U.S.A. 

GRUNE& STRA1TON, INC. 


New York, N. Y. 10016 

Concise . . . Practical 

Clinical 

ARCHIVES OF INTERNAL MEDI- 

CINE, reviewing Dr. Atamer’s 

book, said: 

“The purpose in writing this 

book was to present an up to 

date, concise review of clinical 

hematology for medical students 

and practicing physicians. In the 

finished product, the author has 

achieved this goal . . . a most 

useful feature is the review table 

following each disease.. . . These 

tables should be of great value 

to hematologists as well as to 

other readers. In the text, each 

blood disease is discussed with 

an introduction and tinder the 

headings of physiology, clinical 

and laboratory manifestations, 

diagnosis, prognosis, pathology 

and treatment.” 

BLOOD 

DISEASES 

By M. A. Atamer, M.D. 

G!4 paqes #{149}Many Charts #{149}$16.50 

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New York, N. Y. 10016

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Slanted 

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design permits 

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The upper shoulder is built 

slightly on the bias. One outlet is 

higher than the other. The plasma 

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the upper port. Here they can be 

drawn off with less mixing or loss. 

Similarly (centrifuged upside 

down), packed red cells can be 

drawn off more completely from 

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Or, when the Ph apak is suspended 

for administering whole blood, it 

drains more readily. 

Universal design 

Note also that the Phiapak outlets 

are universal in design: they will 

accept any make of blood administration 

set. Thus filled Pliapaks 

can be freely exchanged between 

one bank or hospital and another, 

regardless of any difference in administration 

set in stock. This is 

more than a cony enience. It is a 

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The Pliapak and its companion 

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thinW ailed needle for 

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the 

The slant makes 

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donor tubingwithstands 

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PLIAPAK Available in 500-mi., 450-ml., and 225.inl. sizes with ACD solution. 

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TRANSPAK#{174} These are Abbott’s empty transfer containers, in 150-ml., 300- 

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BLOOD: THE JOURNAL OF HEMATOLOGY xv 

Report on the Ninth 

Congress of the European 

Society of Hematology 

Lisbon, August, 1963 

The report of this important meeting 

-comprising more than 100 papers 

in both French and English, covering 

all areas of modern’ hematological 

research-has been published by 

San gre, the Spanish journal. 

400 pages . illustrated #{149} $10.00 

THE 

PRO 

Simpifies 

technique, 

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LAB-TEK 

THROMB1N 

SYSTEM 

It is available in the United States 

from 

Intercontinental 

Medical 

Book Corporation 



Raw 

Liver 

Dehydrated - Defatfed 

Concentration 4#{189} raw 

Powder and Tablet Form 

tissue 

Rawness measured by: 

(1) heat coagulable water solubles 

(2) enzyme content 

Raw liver - in treatment of pernicious 

anemia (Minot and Murphy) is only one 

of many indications for raw liver. 

Hematologists recognize that raw liver 

contains significant unidentified nutritional 

values for treatment of blood diseases. 

r Geriatric Medicine, Steiglitz, Chapter 13, “Diseases ot the 

I Blood.” page 207, “. . . whole liver, about two to three 

I pounds a week, is ot value in chronic lymphatic type” 

I (leukemia JI. vi Lab. & CIa. Med. page 743, May. 1956. 

I Grayzel. et al . VioBin raw liver effective in treatment of 

References: -1 amyloidosis Amer JI. Physiology, 157. 2. 1949, Newman, 

I Grossman and toy. VioBirr raw liver regenerated liver 

I lobes as effectively as raw liver and more rapidly than 

I cooked liver J A M A 104, page 564, 1935, Raw liver as 

L supplementary treatment in amebiasis. 

Raw liver, per se, is usually rejected by 

the patient. Raw liver (VioBin) is concentrated 

by removing fat and moisture, 

and is easily tolerated. 

VIOBIN 

LABORATORIES 

Monticello, Illinois 

Only half the normal amounts of plasma and 

reagent are required with the economical 

Lab-Tek Prothrombin System. 

Load the Temp-Control Block with disposable 

reaction chambers. When constant 37#{176}C 

temperature is being maintained, pipet 0.1 

ml thromboplastin-calcium chloride reagent 

into pointed end (or finger side) of reaction 

chamber, and 0.05 ml patient plasma in 

rounded, elevated end. Allow 60 seconds for 

thermal equilibrium, remove chamber from 

block, tilt to spill thromboplastin over the 

dam into the plasma. . . - start stop watch. 

Rock chamber back and forth to mix. 

end point (clot formation) is dramatic and 

immediately visible. Results are consistently 

accurate and reproducible. 

The Lab-Tek Prothrombin System assures 

uniform results at lower cost. Ask your Lab- 

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write. 

LAB-TEK 

WESTMONT, 

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Xvi BLOOD: THE JOURNAL OF HEMATOLOCY 

AN Rh-Hr 

“This book should be a valuable source 

2nd 

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THEIR APPLICATIONS ULTRAMICROMETHODS 

Second Edition, for 

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Director of Pathology Dept. 

and Irving B. Wexler, M.D. Providence Hospital, Detroit, Mich. 

Roderick P. MacDonald, Ph.D. 

FROM REVIEWS OF THE FIRST EDITION: Director of Clinical Chemistry 

- - an up-to-date summary of the complex Harper Hospital, Detroit, Mich. 

subject of Rh types . - . a clear and easily 

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BLOOD: THE JOURNAL OF HEMATOLOGY xvii 

\oarning : This drug is offered for use onl iii acute life-threatening situations 

where hieiiiorrhage results from an overactivity of the fibrinolytic system. 

AMICAR#{174} 

Aminocaproic Acid 

An entirely different agent for the control of 

bleeding by stabilizing blood-clot formation 

What it is-and what it is not 

AMICAR Aminocaproic Acid is an historic 

break-through in the control of bleeding because 

it is the first systemic agent that stabilizes bloodclot 

formation. It is different in chemical makeup 

and pharmacologic action from any other drug 

or entity now available for the control of bleeding. 

It is unique in its action, and does not produce 

its effect by mechanisms available up to now 

to control runaway bleeding. In contrast to other 

agents. it does not act by promoting intravascular 

clot formation; does not act by time-consuming 

strengthening of the capillary walls; does not 

act by establishing a mechanical block; unlike 

vitamin K analogues it does not act on the direct 

formation of fibrin; and it is not a replacement 

for fibrinogen or any other naturally occurring 

substance essential to normal blood coagulation. 

AMICAR is closely related to lysine, but lacks 

the -amino group. It is absorbed rapidly following 

oral intake; and it is excreted rapidly, 

most of it unmetabolized, whether administered 

orally or intravenously. 

And highly important - AMICAR is relatively 

non-toxic. It is rapidly excreted in practically 

unmetabolized form. It does not appear to interfere 

with essential metabolic processes. 

AMICAR Aminocaproic Acid 

inhibits 

fibrinolysiscontrols 

bleeding 

AMICAR controls excessive bleeding by blocking 

one of the first crucial events in the chain of 

chemical reactions leading to clotting-failure: it 

inhibits the activation of plasminogen to prevent 

the formation of plasmin. and to a lesser extent. 

inhibits plasmin itself.”3 

Hyperfibrinolysis - a major 

cause of excessive bleeding 

In normal blood-clotting, fibrinogen is converted 

to fibrin monomers which polymerize to 

form larger groups; these later undergo gelation 

to produce the clot. But when the plasminogen-plasmin 

enzyme system is disturbed, so that 

there is excessive plasmin, the normal bloodclotting 

mechanism goes awry. \Vith fibrinogen 

lvsed by plasmin, disorganized and unstable 

clots are formed that dissolve spontaneously. The 

result is excessive bleeding. Such hyperfibrinolysis 

may he associated with various surgical procedures, 

hematological disorders, neoplastic diseases, 

hepatic cirrhosis, and abruptio placentae. 

References: 

1. Celander, D. R., Nascbke, M. D., and Guest, M. 

M.: The effect of c’aminocaproic acid on fibrinolysin 

and on activators of profibrinolysin. Texa.s Rep. 

Biol. Med. 19:50, 1961. 2. Ablondi, F. B., Hagen, 

J. J., Philips, M., and DeRenzo, E. C.: Inhibition of 

plasmin, trypsin, and the streptokinase-activated 

fibrinolytic system by e-aminocaproic acid. Arch. 

Biochem. 82:153, 1959. 3. Alkjaersig, N., Fletcher, 

A. P., and Sherry, S.: c-aminocaproic acid: An inhibitor 

of plasminogen activation. I. Biol. Chem. 

234:832, (Apr.) 1959. 4. Sjoerdsma, A., and Nilsson, 

I. M.: Aliphatic amino compounds as inhibitors 

of plasminogen activation. Proc. Soc. Exp. 

Biol. Med. 103:533, 1960. 5. Doleschel, W., Auerswald, 

W., and von L#{252}tzow, A.: On the inhibiting 

effect of aminocaproic acid upon the fibrinolytic 

system during “spontaneous activation.” Thromb. 

Diath. Haernorrh. 8:101, 1962. 

Text of official brochure on fifth and sixth pages following

xviii BLOOD: THE JOURNAL OF HEMATOLOGY 

AMICAR#{174} 


Effective control of hyperfibrinolytic 

hemorrhage in open heart surgery 

Hemorrhage on the increase 

in cardiac operations 

The spectacular success of open heart surgery in 

recent years has led to a steady increase in the 

number of operations to correct cardiac defects. 

Impressive as the results have been, many of 

these operations have been accompanied by lifethreatening 

hemorrhage because of the use of 

the pump oxygenator. Incoagulable blood and 

generalized oozing and bleeding may occur quite 

suddenly late in the operation, or in the early 

postoperative 

period. 

Prominent among the coagulation defects observed 

after cardiac bypass of the circulation is 

considerable plasminogen-activation, which is 

frequently related to the duration of the bypass 

procedure. While there are many factors responsible 

for uncontrollable bleeding, experience 

with AMICAR Aminocaproic Acid indicates that 

excessive fibrinolysis is a major contributing 

cause.6 

Gans and Krivit7 investigated the effect of 

AMICAR on a group of patients undergoing 

openIiiit surgery, and the results were com 

pared with those in a similar group of patients 

not receiving this drug. While fibrinolytic activity 

was absent in the plasma of patients pre-treated 

with AMICAR, there was considerable fibrinolytic 

activity in the plasma of patients not receiving 

the drug - proof that this agent was an 

effective inhibitor of plasminogen-activator in 

patients undergoing open heart surgery. On several 

occasions it was noted that with this drug in 

patients with post-cardiac-by pass hemorrhage, 

there was normal clot formation, which had been 

absent before the administration of the drug. 

Kirklin8 treated approximately 25 patients 

with AMICAR after cardiac surgery. In all these 

patients, bleeding - either in the operating room 

or in the postoperative period-was so substantial 

as to be a grave threat to survival. Three-fourths 

of the patients treated benefited from this drug. 

Rodenbaugh#{176} described the dramatic effect of 

AMICAR in a man who developed an extreme 

degree of circulating fibrinolysin during aortic 

surgery. In spite of vigorous local methods of 

control, hemorrhage was continuing at a rapid 

rate, with lysis of the whole-blood clot occurring 

within ten minutes. Five grams of AMICAR were 

given rapidly, five grams over the next two hours, 

and another five grams over the next twelve 

hours. Fibrinolytic activity and hemorrhage 

ceased within fifteen minutes after this regimen 

was initiated. 

References: 

6. Sweeney, W. M.: Epsilon-aminocaproic acid, an 

inhibitor of fibrinolysis. To be published. 7. Gans, 

H and Krivit, W.: Problems in hemostasis during 

open.heart surgery. III. Epsilon.aminocaproic acid 

as an inhibitor of plasminogen activator activity. 

Ann. Surg. 155:268, Feb., 1962. 8. Kirklin, J. W.: 

Report to Lederle Laboratories. 9. Rodenbaugh, 

F. H.: Report to Ledorle Laboratories.

BLOOD: THE JOURNAL OF HEMATOLOGY xix 

Controls surgical and nonsurgical bleeding 

of the urinary tract 

Urinary fibrinolysis is usually a normal physiological 

phenomenon, mediated by the enzyme 

urokinase, which helps preserve the patency of 

excretion pathways. But with severe trauma or 

shock, such as surgery, this fibrinolysis may result 

in surgical hematuria-a common occurrence 

after prostatectomy or nephrectomy. Non-surgical 

hematuria often accompanies polycystic 

or neoplastic diseases of the kidneys. Systemic 

hyperfibrinolysis, a pathologic condition, may 

result from carcinoma of the prostate as well as 

other organs. 

Post-prostatectomy 

loss reduced with 

blood 


Blood loss following prostatic resection is so 

familiar that it has almost been taken for granted. 

Such blood loss, however, has been shown to 

range from 200 cc. to 1800 cc. in a series of 

patients during and after transurethral surgery.’0 

Hemorrhage of this magnitude could be 

quite dangerous in elderly patients. 

A new addition to the agents for reducing 

blood loss in this type of surgery is AMICAR 

Aminocaproic Acid. The following controlled 

studies have demonstrated its efficacy: 

1. McNicol et al.:’#{176}In a comparison of 9 suprapubic 

prostatectomy patients treated with this 

agent, with 8 similar patients as controls, blood 

loss in the treated patients was less than half that 

in the controls. In a comparison of 13 transurethral 

prostatectomy patients treated with this 

agent, with 15 nontreated patients as controls, 

there was only one fourth as much bleeding in 

those getting AMICAR as in the controls. This 

reduction was most marked on the first day of 

treatment. The drug was later given to another 

group of patients in whom hematuria was so 

severe or protracted as to cause concern. All but 

one of these showed a beneficial effect. 2. Fetter 

et al.:” Patients treated with AMICAR lost 

significantly less blood in the first 24 hours after 

prostatectomy than did untreated controls. This 

facilitated earlier removal of drainage tubes and 

a shortened period of hospitalization. 3. Sack 

et al. :12 Fifty-six patients were randomly assigned 

to either saline placebo or AMICAR after 

prostatectomy. The reduction i,postoperative 

bleeding in those receiving the drug was statistically 

and clinically significant. 4. Andersson 

and Nilsson :‘ Blood loss was compared in two 

groups of patients during the first three days 

after prostatectomy. The average blood loss 

among those treated with AMICAR was 132 ml., 

compared with 449 ml. in those not receiving 

this drug. 


controlled hemorrhage in 

prostatic 

carcinoma 

In a group of patients with prostatic cancer 

complicated by hemorrhage, AMICAR regularly 

reduced or completely controlled bleeding.’3 In 

a patient with prostatic carcinoma who had hemorrhiage 

related to severe hypofibrinogenemia, 

bleeding was controlled by periodic intravenous 

infusions of AMICAR.’4 Another patient with 

prostatic carcinoma, who had fibrinolytic bleed. 

ing following cystoscopy, was treated with this 

agent orally; the plasminogen-activator substance 

was inhibited.’5 

References: 

10. McNicol, G. P., Fletcher, A. P., Alkjaersig, N., 

and Sherry, S.: The use of epsilon-aminocaproic 

acid, a potent inhibitor of fibrinolytic activity in 

the management of postoperative hematuria. I. 

Urol. 86:829, 1961. 11. Fetter, T. R., Tocantins, L. 

M., Cottone, R. N., Brosseau, C., and Bowman, W. 

B.: Effect of epsilon-aminocaproic acid on bleeding 

after prostatectomy, I. Urol. 85:970, (June) 

1961. 12. Sack, E., Spaet, T. H., Gentile, R. L., 

and Hudson, P. B.: Reduction of postprostatectomy 

bleeding by epsilon.aminocaproie acid. 

New Eng. I. Med. 266:541, (Mar. 15) 1962. 13. Andersson, 

L., and Nilsson, I. M.: Treatment of fibrinolytic 

states in prostatic disease with E-ACA. Proceedings 

of the Eighth Congress of the European 

Society of Hematology, Vienna, 1961, Part II, p 

452. 14. Rodenbaugh, F. H.: Report to Lederle 

Laboratories. 15. Malcolm D., and O’Connor, J. J.: 

Generalized fibrinolytic bleeding following cystoscopy 

in a patient with carcinoma of the prostate. 

I. Urol. 90:458, (Oct.) 1963.

xx BLOOD: THE JOURNAL OF HEMATOLOGY 

AMICAR#{174} 


Effectively controlled hyperfibrinolytic bleeding 

in abruptio placentae 

Effectively controlled 

hyperfibrinolytic bleeding in 

abruptio placentae 

“Hemorrhage currently is the principal cause 

of maternal mortality,” according to Phillips,16 

having displaced infection as the leading cause. 

And, as Ratnoff’7 points out, it has become increasingly 

apparent that disorders of blood coagulation 

are usually present when uterine bleeding 

is fatal. Probably the most frequent cause 

of excessive blood loss in pregnancy is premature 

separation of the placenta. 

Roth’8 administered AMICAR Aminocaproic 

Acid (5 Gm. intravenously) to 56 patients with 

excessive bleeding immediately after expulsion 

of the placenta or in the puerperium. In 44 of 

these patients (78.6%), who had hemorrhage 

associated with such conditions as surgical delivery, 

protracted and difficult second stage, manual 

separation of the placenta, etc., hemostasis 

occurred within a few minutes after injection of 

this agent. In the 12 patients who failed to 

respond to this treatment, the continued bleeding 

resulted from vaginal or cervical tears, hyperplastic 

decidual endometritis, and placental 

polyp. 

Similar findings, but on fewer patients, have 

been reported by other investigators. Tobin1#{176} 

treated with AMICAR two patients from the 

obstetric service who ad marked hypofibrino. 

genemia. Additional treatment consisted of fibrinogen 

and whole blood. There was not only a 

striking rise in fibrinogen levels, but there was 

also inhibition of fibrinolytic activity. 

Tench2#{176} has reported on the life-saving use of 

AMICAR in a patient with abruptio placentae. 

The patient was admitted to the hospital for delivery 

with moderate vaginal bleeding which 

later became severe. A laboratory report indicated 

“no fibrinogen,” and the patient later went 

into severe shock. AMICAR was administered 

intravenously, followed by fibrinogen, with a 

repeat dosage of the former agent. The following 

morning, the fibrinogen level was normal, and 

recovery was uneventful. 

In the case of another patient with abruptio 

placentae, who had profuse bleeding and a 

severe fibrinolytic process, Fisher2’ administered 

AMICAR, with the result that the fibrinolysis 

was haTid. The response to this agent, according 

to the investigator, was quite impressive. 

References: 

16. Phillips, 0. C.: Maternal mortality: The fallacy 

of the irreducible minimum. W. Virginia Med. I. 

59:147, 1963. 17. Ratnoff, 0. D., Pritchard, J. A., and 

Colopy, J. E.: Hemorrhagic states during preg. 

nancy. New Eng. I. Med. 253:63, (July 14) 1955. 

18. Roth, F.: Orientation in the use of epsilonaminocaproic 

acid in obstetrics and gynecology. 

Ther. Umsch. 9:358, (Sept.) 1962. 19. Tobin, J. R.: 

Clinical Report to Lederle Laboratories, March 27, 

1961. 20. Tench, W. R.: Clinical Report to Lederle 

Laboratories, Feb 8, 1962. 21. Fisher, L. M.: Clinical 

Report to Lederle Laboratories, Feb. 15, 1962. 

Text of official brochure follows

BLOOD: THE JOURNAL OF HEMATOLOGY xxi 

Controls spontaneous bleeding associated 

with cirrhosis of the liver 

That fibrinolysis is associated with hepatic insufficiency 

has long been known; that hyperfibrinolysis 

in liver diseases may be more common than 

generally realized was shown by Grossi et al.22 

These investigators demonstrated abnormal spontaneous 

fibrinolytic activity in the plasma of 

about half of a series of 51 patients with severe 

cirrhosis of the liver. In 15 of these patients, 2 

grams of AMICAR Aminocaproic Acid given by 

intravenous infusion brought a rapid decrease in 

spontaneous fibrinolytic activity to normal levels, 

which lasted from 2 to 4 hours after the end of 

infusion. In the same 15 patients, with abnormally 

increased spontaneous whole blood clot 

lysis, this agent produced a definite and prolonged 

inhibition of the lysis. A patient with 

severe cirrhosis and hyperfibrinolysis, who had 

severe, persistent bleeding after a dental extraction, 

was given AMICAR by intravenous infusion. 

The fibrinolytic activity decreased and the 

bleeding stopped. Although bleeding resumed 

after the effect of the agent wore off, it stopped 

again following a second administration. More 

recently Grossi et al.23 found AMICAR useful 

in the arrest and control of abnormal oozing in 

patients with cirrhosis of the liver undergoing 

portasystemic shunt, with a reduction in operative 

mortality. 

References: 

22. Grossi, C. E., Moreno, A. H., and Rousselot, L. 

M.: Studies on spontaneous fibrinolytic activity in 

patients with cirrhosis of the liver and its inhibition 

by epsilon-aminocaproic acid. Ann. Surg. 153:383, 

(Mar.) 1961. 23. Grossi, C. E., Rousselot, L. M., and 

Panke, W. F.: Hemorrhagic diatheses during and 

after portacaval shunts in patients with cirrhosis of 

the liver; their recognition and management. Am. 

J. Gastroent. 41:117 (Feb.) 1964. 

Official 

AMICAR Aminocaproic Acid; 6-Aminocaproic 

Acid: Intravenous, Syrup, and Tablets. 

Warning 

THIS DRUG IS OFFERED FOR USE ONLY IN ACUTE 

LI FE-THREATEN! NG SITUATIONS WHERE HEMOR- 

RHAGE RESULTS FROM AN OVERACTIVITY OF THE 

FIBRINOLYTIC 

SYSTEM. 

AMICAR Aminocaproic Acid has a very specifi 

action in that it inhibits both plasminogen 

activator substances and, to a lesser degree, plasmm 

activity. The drug should NOT be administered 

without a definite diagnosis, and/or laboratory 

findings indicative of hyperfibrinolysis 

(hyperplasminemia) . 

Animal experiments indicate particular caution 

should be taken in administering AMICAR 

Aminocaproic Acid to patients with cardiac, 

hepatic or renal diseases. 

Demonstrable animal pathology in some cases 

have shown endocardial hemorrhages and myocardial 

fat degeneration. The use of this drug 

should thus be restricted to patients in whom the 

benefit hoped for would outweigh the hazard. 

Rapid intravenous administration of the drug 

should be avoided since this may induce hypotension, 

bradycardia and/or arrhythmia. 

One case of cardiac and hepatic lesions observed 

in man has been reported. The patient 

received 2 grams of aminocaproic acid every 6 

hours for a total dose of 26 grams. Death was 

due to continued cerebral vascular hemorrhage. 

Necrotic changes in the heart and liver were 

noted at autopsy. 

If it is accepted that fibrinolysis is a normal 

Brochure 

process, potentially active at all times to ensure 

the fluidity of blood, then it must also be accepted 

that inhibition of fibrinolysis by aminocaproic 

acid may result in clotting or thrombosis. However, 

there is no definite evidence that administration 

of aminocaproic acid has been responsible 

for the few reported cases of intravascular clotting 

which followed this treatment. Rather, it 

appears that such intravascular clotting was 

most likely a result of the fibrinolytic disease 

being treated. 

It has been postulated that extravascular clots 

formed in vivo with incorporated aminocaproic 

acid may not undergo spontaneous lysis as do 

normal clots. However, it is the consensus of 

experts that the few reported cases of extravascular 

clotting could have occurred in the absence 

of aminocaproic acid treatment. 

Description 

AMICAR Aminocaproic Acid Lederle is a 

monaminocarboxylic acid which acts as an effective 

inhibitor of fibrinolysis. 

Site and Mode of Action 

The beneficial fibrinolysis-inhibitory effects of 

AMICAR Aminocaproic Acid appear to be mediated 

principally via inhibition of plasminogen 

activator substances and, to a lesser degree, 

through antiplasmin activity. The drug is absorbed 

rapidly following oral administration. 

Whether administered by the oral or intravenous 

route a major portion of the compound is recovered 

unmetabolized in the urine. The renal 

clearance of AMICAR Aminocaproic Acid is 

high (about 75 per cent of the creatinine clear-

xxii BLOOD: THE JOURNAL OF HEMATOLOGY 

ance). Thus the drug is excreted rapidly. After 

prolonged administration AMICAR Aminocaproic 

Acid distributes throughout both the extravascular 

and intravascular compartments of the 

body and readily penetrates human red blood 

and other tissue cells. 

Indications 

AMICARAminocaproic Acid has proved 

useful, in many instances, in the treatment of 

excessive bleeding which results from systemic 

hyperfibrinolysis and urinary fibrinolysis. In lifethreatening 

situations, fresh whole blood transfusions, 

fibrinogen infusions, and other emergency 

measures may be required. 

Systemic hyperfibrinolysis, a pathological condition, 

may frequently be associated with surgical 

complications following heart surgery (with 

or without cardiac bypass procedures) and portacaval 

shunt; hematological disorders such as 

aplastic anemia; abruptio placentae; hepatic cirrhosis; 

neoplastic disease such as carcinoma of 

the prostate, lung, stomach, and cervix. 

Urinary fibrinolysis, usually a normal physiological 

phenomenon, may frequently be associated 

with life-threatening complications following 

severe trauma, anoxia, and shock. Symptomatic 

of such complications is surgical hematuna 

(following prostatectomy and nephrectomy) 

or nonsurgical hematuria (accompanying polycystic 

or neoplastic diseases of the genitourinary 

system). 

Contraindications 

AMICAR Aminocaproic Acid should not be 

used when there is evidence of an active intravascular 

clotting process. The effect of AMICAR 

Aminocaproic Acid on the fetus and transplacental 

passage of this drug is unknown. Therefore 

its use during the first and second trimesters 

of pregnancy should be coafined to instances 

where need outweighs possible hazards. 

Side Effects 

Occasionally nausea, cramps. diarrhea, dizziness. 

t innitus, malaise, conjunctival suffusion, 

nasal stuffiness, headache, and skin rash have 

been reported as results of the administration 

of aminocaproic acid. Only rarely has it been 

necessary to discontinue or reduce medication 

because of one or more of these effects. 

Thrombophiebitis. a possibility with all intravenous 

therapy, should be guarded against by 

strict attention to the proper insertion of the 

needle and the fixing of its position. 

Dosage Forms 

AMICAR Aminocaproic Acid Ledenle Intravenous. 

Each 20 cc. vial contains 5.0 Gm. of 

Aminocaproic Acid (250 mg. per cc.) as an aqueous 

solution, with 0.08% methylparaben and 

0.02% propylparaben as preservatives. 

AMICAR Aminocaproic Acid Lederle 25% 

Syrup. Each cc. of syrup contains 250 mg. of 

Aminocaproic Acid with 0.1% Sodium Benzoate 

and 0.2% Potassium Sorbate as preservatives. 

AMICAR Aminocaproic Acid Lederle Tablets. 

Each tablet contains 500 mg. of Aminocaproic 

Acid. 

Administration and Dosage 

Initial Therapy: An initial priming dose of 5 

grams of AMICAR Aminocaproic Acid administered 

either orally or intravenously followed 

by 1 to 11/4 gram doses at hourly intervals thereafter 

should achieve and sustain plasma levels 

of 0.130 mg./ml. of the drug. This is the concentration 

apparently necessary for the inhibition 

of systemic hyperfibrinolysis. Administration 

of more than 30 grams in any 24-hour period is 

not recommended. 

Intravenous: AMICAR Aminocaproic Acid 

Intravenous is administered by infusion, utilizing 

the usual compatible intravenous vehicles (e.g. 

Water for Injection, physiologic saline, 5% dextrose 

or Ringer’s Solution). RAPID INJECTION OF 

AMICAR AMINOCAPROIC ACID INTRAVENOUS UN- 

DILUTED INTO A VEIN IS NOT RECOMMENDED. 

For the treatment of acute bleeding syndromes, 

it is suggested that 16 to 20 cc. (4 to 5 grams) of 

AMICAR Aminocaproic Acid Intravenous be administered 

by infusion during the first hour of 

treatment, followed by a continuing infusion at 

the rate of 4 cc. (1.0 gram) per hour. This 

method of treatment would ordinarily be continued 

for about 8 hours or until the bleeding 

situation has been controlled. 

Oral Therapy: If a patient is able to take 

medication by mouth, an identical dosage regimen 

may be followed by administering AMICAR 

Aminocaproic Acid Tablets or 25% Syrup as 

follows: For the treatment of acute bleeding syndromes, 

due to elevated fibrinolytic activity, it is 

suggested that 10 tablets (5 grams) or 4 teaspoonfuls 

of syrup (5 grams) of AMICAR 

Aminocaproic Acid be administered during the 

first hour of treatment, followed by a continuing 

rate of 2 tablets (1 gram) or 1 teaspoonful of 

syrup (11/4 grams) per hour. This method of 

treatment would ordinarily be continued for 

about 8 hours or until the bleeding situation has 

been controlled. 

5Stefanini, M. and Dameshek, W.: Hemorrhagic Disorders 

Ed. 2, New York, Grune an(l Stratton, pp. 

510-514, 1962. 

The use of AMICAR Aminocaproic Acid should be 

accompanied by tests designed to (letermine the 

amount of fibrinolysis present. There arc presently 

available (a) general tests, such as those for the 

determination of the lysis of a clot of blood or plasma 

and ib) more specific tests for the study of various 

phases of fibrinolytic mechanisms. These latter tests 

include both semi-quantitative an(l quantitative techniques 

for the determination of pro-fibrinolysin, 

fibrinolysin. an(l anti-fibrinolysin. 

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BLOOD: THE JOURNAL OF HEMATOLOGY xxix 

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BLOOD: THE JOURNAL OF HEMATOLOGY 

An invaluable new monograph 

The CLINICAL USE 

OF DEXTRAN SOLUTIONS 

By Arnie! Sega! 

Walter Reed Army Medical Center, Walter Reed Army Institute 

of Research, Department of hematology, Washington, D. C. 

Present address: University of Pennsylvania School of Medicine. 

With a foreword by William H. Crosby, Colonel, 

Medical Corps, United States Army 

In the past thirty years, physicians have tried many substances as plasma 

volume expanders, only to discard them for one reason or other. Today, 

dextran, a polymer of dextrose, has proved to be the most acceptable of the 

expanders used in the United States. 

Now, with the imminent introduction in this country of a new form, low 

molecular weight dextran (LMWD), this substance seems likely to find even 

greater use. As Dr. William Crosby says in the preface to this book, “. . . its 

ability to improve perfusion of the microcirculation may provoke a small 

revolution in management of problems of acute vascular impairment.” 

But dextran, for all its usefulness, has its drawbacks. For one thing, the 

concentrated dextran in solutions may continue to expand the volume after 

infusion is completed. Thus, any physician who uses dextran must know its 

characteristics and indications for use. 

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It is the result of an extensive review of clinical experience with dextran 

performed very capably by the author at the request of the Office of the 

Deputy Assistant Secretary of Defense (Health and Medicine). 

TABLE OF CONTENTS 

Introduction 

Fate of Injected Dextran 

Effects of Infusions of Clinical Dextrans upon the Organism 

Therapeutic Experiences with Infusion of Clinical Dextran 

Low Molecular Weight Dextran 

80 pages #{149}6 illustrations #{149}$4.50 

CRONE&STRA1TON, INC. ‘t:

cxxvii BLOOD: THE JOURNAL OF HEMATOLOGY 

EFFECTIVE 

IN DETECTING ANTIBODIES ALREADY KNOWN 

EFFECTIVE 

IN DETECTING NEW ANTIBODIES 

CONTRO LLED 

SENSITIVITY is the 

key feature behind 

KNICKERBOCKER 

COOMBS SERUM 

REVIEW THE RECORD OF OUTSTANDING EFFECTIVENESS I 

KNICKERBOCKER COOMBS SERUM PARTiCIPATED IN.. 

“T5r’ anti-V detecting the first anti-V.’ 

1955 Fy(a-b-) 

establishing first phenotype 

Duff y (Fy(a-b-D.’ 

anti-penicillin 

discovering anti-penicillin 

1957 

antibody 

antibody.’ 

confirming the first phenotype 

1958 ik(a-b-) Kidd ik(a-b-) plus the antibody 

combination anti-ik’, Jk.4 

anti-Kp5 

identifying the first pure 

anti-Kp5 (Rautenberg).’ 

anti-Lu5 

describing the third example 

of anti-Lu5 (Lutheran),’ 

1959 anti-Ge 

identifying the second example 

of anti-Ge (Gerbich),’ 

1960 anti-Di 

detecting the fourth example 

of anti-Di’ (Diego),B 

anti-VS 

describing the first 

of anti-VS.’ 

example 

1961 

establishing 

linked blood 

the first sex- 

group system tXg’).’#{176} 

‘ 

1962 anti-is5 

describing the second example 

of anti-is5 (Sutter).’ 1 

REFERENCES I. DeNatale, A., et at.: IA MA j5:247, 1955. 2. Singer, 5., et at: Br)?. 3. 

of Haematology j370 Oct) 1955 3. icy. A B., et al.. Scent, 53.71118 (Mi, 9) 19S0 

4. lack. 1 A and Lies. A. Amer Med. Technology (Ma,c -Ap:() 1960, p. 141 

. B I 

5 Ande,son, L, ci al. Amer J Med. Technology (Map-June) 1959, p. 184 6 Data o’ 

f:ie w:th kn.cke,bocker B:o)og:cs, New York, N.Y. 7. Rosenf:eld, B. E., ci a) Brit. J. 

Haematoiogy Vl:344 Oct (1960. 8. Van Peenen, H. J., ci a).: Blood 17 457 (Apr:)) 1961 

9. Singer’ et al. Nature 196.171 (Apr:) 9)1960. 10. Mann, J. D.T0t a) The Lance?, 

B., 

la 8 Jan. 6) 1962. 11. DaTion file with Kn:ckerbocker B:o)og:cs, New York, BY. 

KNICKERBOCKER COOMBS SERUM 

for more complete antibody coverage 

available in 5 ml. & 10 ml, sizes 

To order or have your Pfizer representative 

call, write: 

[1(X)KNICKERBOCKER BIOLOGICS 

Pfizer Laboratories Dinision/Chas, Pfizer & Co.. Inc. 

300 West 43rd Street, New York, N.Y. 10036

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